Essential hypertension is generally attributed to the interaction of a genetic predisposition and environmental influences. The relative contributions of genetic and environmental factors and the nature of the interactions between them remains poorly understood. Heredity clearly influences the development of essential hypertension, as well as its manifestations. It is highly unlikely, however, that a single gene mutation accounts for the broad pathophysiologic spectrum of essential hypertension. Blood pressure regulation occurs through numerous physiological and biochemical pathways, each presumably with its own genetic control. Many hypertensive patients, for instance, appear to have a renal defect causing delayed excretion of a sodium load (salt-sensitivity). Others exhibit exaggerated pressor response to environmental stimuli (vascular hyper reactivity), or inappropriately high renin secretion (high renin hypertension). Each of these hypertension phenotypes likely represents different inherited pathophysiological predilections that, given the appropriate environmental stimulus (e.g. high sodium intake) leads to a common clinical manifestation (elevated blood pressure). In order to elucidate the genetic basis of essential hypertension, it is necessary to correlate these phenotypes with specific genotypes. Thus, the purpose of this study is to investigate the genetic basis of essential hypertension and salt sensitivity in African American men and women. We hypothesize that genetic variability in the adrenergic receptors leads to salt sensitivity, and thus to the pathogenesis of hypertension in many blacks. We are testing this hypothesis using robust sib-pair analysis, with the adrenergic receptors as candidate genes for the phenotype salt sensitivity. The significance of this study is the potential for identifying genes responsible for high blood pressure in African Americans.